Teixobactin works by binding lipid precursors of the cell wall. This interference weakens the bacterial cell wall, causing the microbes to leak and die. The drug is only effective against gram-positive bacteria, like Staphylococcus aureus and M. tuberculosis, and it could help combat resistant strains that commonly cause MRSA infections. Teixobactin was active against MRSA infections in mice. It is not effective on gram-negative bacteria, like E. coli.

The method they used to discover the antibiotic is also quite interesting. Compound Interest explains:

We know bacteria produce their own antibacterial compounds, to combat other competing bacteria. However, since 99% of bacteria can’t be grown in lab conditions, this greatly limits the number of these compounds that we can investigate. The method used to discover teixobactin overcomes this, by diluting soil samples, then placing small samples containing single bacterium cells in a device they named an ‘iChip’.

The ‘iChip’ is essentially just a device with a large number of small channels, into which bacteria can be deposited. The channels are then covered with a semi-permeable membrane, which allows environmental factors which influence bacterial cell growth to diffuse across to the bacterium cells. Using this method, the researchers were able to cultivate bacteria which were not previously grown in lab conditions, as once a culture is formed it is easier to entice them to do so. The researchers isolated 25 different antibiotic compounds, of which teixobactin is the most promising.

Science magazine reports on a study lending support to the existence of a gene for homosexuality. The study, led by J. Michael Bailey and Alan Sanders, was published this week at Psychological Medicine. The scientists analyzed the genomes of 409 pairs of gay brothers from 384 different families. A genome-wide linkage scan led to the identification of two potential markers, one on chromosome Xq28 (which had been reported in a previous smaller study) and another in a region of chromosome 8. Bailey, for one, was surprised to find any linkage:

Bailey says he went into the project skeptical, largely because Hamer had studied just 38 pairs of gay brothers. “I thought that Dean did a fine but small study, but if I had to bet, I would have bet against our being able to replicate it.”

If you don’t see gay people celebrating this news in the streets, understand that we’ve been hearing news about a potential biological basis for homosexuality for a long time now. In 1991, neuroscientist Simon LeVay suggested that small differences in the size of certain cell clusters in the hypothalamus could influence sexual orientation in men. In 1993, geneticist Dean Hamer published a paper in Science that claimed that genetic markers on the X chromosome could influence the development of a same-sex orientation in men…

As the discipline of genetics changed, so too did the scientific approach to homosexuality. In 2012, scientists examined the possibility that variations in hormone levels in the womb could influence the expression of genes that affect sexual orientation, a line of inquiry that falls under the emerging sub-discipline of epigenetics. The popular media, once so easily convinced by LeVay that homosexuality resulted from brain size and by Hamer that homosexuality was genetic, promptly changed its tune to declare that homosexuality was now epigenetic. Hooray? If it’s hard to get excited about these studies, it’s because, at this point, biological explanations for homosexuality are like iPhones—a new one comes out every year.

Bailey and Sanders acknowledge their work has limitations. Even the strongest linkage on Xq28 wasn’t statistically significant, and genome wide association studies are better at homing in on genes for a trait than the linkage study they performed this time:

Sanders admits that the strongest linkage identified from an isolated genetic marker on Xq28 doesn’t clear the threshold for significance. But he contends that the case is bolstered by neighboring markers, which appear to be shared at higher rates between pairs of gay brothers. “The convergence of the evidence pointed towards” Xq28 and chromosome 8, he asserts.

Bailey and Sanders may soon have more data to back their claim—or refute it. They are now working on a GWA study that includes genetic data from the just-published work plus DNA samples from more than 1000 additional gay men. Based on the results published this week, “it looks promising for there being genes in both of these regions,” Bailey says, “but until somebody finds a gene, we don’t know.”

Meanwhile, the New Scientist worries about the implications of the research:

On the one hand, if sexual orientation is something people are born with, and cannot change even if they want to – akin to skin colour or handedness – this should overturn the notion that people choose to be gay and could equally well choose not to be. That knowledge would help rebut those who suggest that gayness is the result of a morally unacceptable decision, or a psychological disorder. It might also help people who struggle to understand or declare their own homosexuality.

On the other, some could try to redefine homosexuality as a biological abnormality. There is no way to change people’s sexuality, but if key genes are found, it might be possible to detect homosexuality before birth, or to “cure” people by altering those genes.

Comet 67P/Churyumov–Gerasimenko as seen by Philae lander as it lands on the surface.

The European Space Agency (ESA) has made the first landing on a comet in history with their Rosetta mission. The Philae lander touched down on comet 67P/Churyumov-Gerasimenko at around 11AM EST. Philae will be active for about two days, conducting the first in situ analysis of a comet’s surface. Philae’s mothership will orbit and observe the comet through 2015. The objective of the mission is to observe how a frozen comet is transformed by the sun. Learn more about the Rosetta mission on the ESA’s website.

Is Ebola evolving as it continues to spread throughout parts of Western Africa? Researchers in the US and Europe face myriad delays as they try to discover the answer. They believe this information is key to understanding how the virus jumps from animals to humans, and also whether it is becoming more virulent or contagious as it continues to spread. According to Science Magazine, thousands of samples have been sitting untouched as scientists await health ministry approvals to import the virus. In places where samples have been imported, scientists have often left the lab for more important field work, helping to contain the virus where they can.

Several researchers say that getting export approval from beleaguered health ministries has been tough. “I can only assume that the system is so overwhelmed that processing samples beyond simple diagnostic tests is not high priority,” says Rambaut, who was a co-author on the August sequence paper.

Stephan Günther, a virologist at the Bernhard Nocht Institute for Tropical Medicine (BNI) in Hamburg, Germany, and coordinator of the European Mobile Laboratory (EMLab) consortium, says they have been unable to export samples from Nigeria or Liberia. But BNI has been receiving samples from the EMLab mission in Guinea since March and now has close to 3000, he says. (BNI is storing them in its high-security lab on behalf of the Guinean government, which still owns them.)

Günther and his colleagues have not yet sequenced any of the samples, because consortium staff members have been busy supporting diagnostic centers in affected countries. “We are all busy with fieldwork,” Günther says. “Personnel is a bit of a problem.”

As the global panic eases, clearances should begin. The Institut Pasteur hopes to begin sequencing samples from Guinea soon and samples from Sierra Leone destined for the U.S. were cleared last week. Scientists have also begun making preparations to get DNA sequencers to affected countries. The genome, combined with demographic and treatment information will help provide a clear picture of how the outbreak spread, but there would still be a lot more data needed to determine if Ebola is becoming more virulent:

New sequences probably won’t show that the virus is finding new ways to attack or spread, Rambaut says. Instead, the prize is a clearer picture of the outbreak. A cluster of closely related viruses might point to a hotspot of transmission, he says, while unexpectedly diverse sequences would suggest that many cases were going undetected. Sequence data could also help researchers tell whether there has been more than one animal-to-human introduction.

Earlier sequence data did suggest that the virus was undergoing rapid changes, but that is not necessarily a sign that it is becoming more dangerous, Rambaut says. “Most RNA viruses mutate quickly, but adaptation and functional change is a much slower process.” Measles mutates nearly as quickly as Ebola virus, but it has never evolved to escape the lifelong immunity of previously infected or vaccinated individuals. Even in an outbreak this big, Rambaut says, “I see no reason to suspect the virus will radically change its life cycle or its mode of transmission.”

An in-depth study of the cat genome reveals details about their history and behaviors.

An in-depth study of the cat genome highlights a variety of genes, including ones for digesting their meaty diets, keen eyesight and good hearing. The researchers found that pet cats also have genes that allow them to respond to positive reinforcement. From Popular Science:

Cats also seem to have more genes related to digesting fat than other carnivores do, which is important for their super-meaty diets. (Scientists call cats, including wildcats, hypercarnivores.) Cats even have genes that may help them avoid heart disease from their high-fat diets. Polar bear genomes bear similar markers of selection for fat-digesting genes.

To look for the genes influenced by human selection, the researchers analyzed DNA pooled from 23 pet cats, including Cinnamon. They compared the domestic cat DNA with DNA from four wildcats. Among the feline genetic traits that people seem to have chosen are ones that influence how the cat brain responds to rewards. Yep, that means kitty treats! Mice that are missing the mouse versions of some of those genes are poor at learning with food rewards. Perhaps when people first brought cats into their barns and homes, they chose the ones that were more motivated to do things for people in return for tasty tidbits.